[Animal models in lupus].
The study of spontaneous animal models of the lupoid disease has permitted a better understanding of the intermediary mechanisms which lead to the production of auto-anti-polymorphonuclear antibodies, and of glomerulo-nephritis by means of immune complexes. In comparison with a primitive thymic deficiency which causes a disorder in immunity regulation, under the control of activating and suppressing T lymphocytes, these models have demonstrated the probable role of intrinsic hyper-activity of the B lymphocytes. The association of these two disturbances seems necessary for the development of the disease in NZB and F1 New Zealand mice (NZB X NZW); nonetheless, the studies of other murine models (notably MRL/1 pr and B X SB mice) reveal a great diversity in lymphocytic disturbances, capable of leading to the production of auto-antibodies. These models allow genetic control of lupoid disease to be undertaken. Finally, canine lupus and Aleutian mink disease underline the possible role of a transmittable viral agent.
D000453:Aleutian Mink Disease; D000818:Animals; D001323:Autoantibodies / Q000096:biosynthesis; D001402:B-Lymphocytes / Q000276:immunology; D004195:Disease Models, Animal; D004283:Dog Diseases; D004285:Dogs; D005260:Female; D005796:Genes; D006801:Humans; D006824:Hybridization, Genetic; D008180:Lupus Erythematosus, Systemic / Q000209:etiology / Q000276:immunology; D008297:Male; D051379:Mice; D008814:Mice, Inbred NZB; D008815:Mice, Inbred Strains; D008907:Mink; D013601:T-Lymphocytes / Q000276:immunology; D014780:Viruses / Q000472:pathogenicity
D001323:Autoantibodies
Modèles animaux de la maladie lupique.